Varicella zoster virus

Human alphaherpesvirus 3, usually referred to as the varicella-zoster virus (VZV), is one of eight herpesviruses known to infect humans. It causes chickenpox (varicella), a disease most commonly affecting children, teens, and young adults, and shingles (herpes zoster) in adults; shingles is rare in children. VZV is a worldwide pathogen known by many names: chickenpox virus, varicella virus, zoster virus, and Human herpesvirus 3 (HHV-3). VZV infections are species-specific to humans, but can survive in external environments for a few hours, maybe a day or two. Human alphaherpesvirus 3, usually referred to as the varicella-zoster virus (VZV), is one of eight herpesviruses known to infect humans. It causes chickenpox (varicella), a disease most commonly affecting children, teens, and young adults, and shingles (herpes zoster) in adults; shingles is rare in children. VZV is a worldwide pathogen known by many names: chickenpox virus, varicella virus, zoster virus, and Human herpesvirus 3 (HHV-3). VZV infections are species-specific to humans, but can survive in external environments for a few hours, maybe a day or two. VZV multiplies in the lungs, and causes a wide variety of symptoms. After the primary infection (chickenpox), the virus goes dormant in the nerves, including the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Many years after the person has recovered from chickenpox, VZV can reactivate to cause neurologic conditions. Primary varicella zoster virus infection results in chickenpox (varicella), which may result in complications including encephalitis, pneumonia (either direct viral pneumonia or secondary bacterial pneumonia), or bronchitis (either viral bronchitis or secondary bacterial bronchitis). Even when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person (virus latency), in the trigeminal and dorsal root ganglia. VZV enters through the respiratory system. Having an incubation period of 10–21 days, averaging at 14 days. targeting the skin and peripheral nerve, the period of illness is from 3 to 4 days. 1–2 days before the rashes appear, is when this virus is the most contagious. Some signs and symptoms are vesicles that fill with pus, rupture, and scab before healing. Lesions tend to stay towards the face, throat, and lower back sometimes on the chest and shoulders. Shingles usually stay located around the waist. In about 10–20% of cases, VZV reactivates later in life, producing a disease known as shingles or herpes zoster. VZV can also infect the central nervous system, with a 2013 article reporting an incidence rate of 1.02 cases per 100,000 inhabitants in Switzerland, and an annual incidence rate of 1.8 cases per 100,000 inhabitants in Sweden. Other serious complications of varicella zoster infection include postherpetic neuralgia, Mollaret's meningitis, zoster multiplex, and inflammation of arteries in the brain leading to stroke, myelitis, herpes ophthalmicus, or zoster sine herpete. In Ramsay Hunt syndrome, VZV affects the geniculate ganglion giving lesions that follow specific branches of the facial nerve. Symptoms may include painful blisters on the tongue and ear along with one sided facial weakness and hearing loss. If infected during initial stages of pregnancy severe damage to the fetus can take place. Reye’s syndrome can happen after initial infection, continuous vomiting and shows signs of brain dysfunction: extreme drowsiness or combative behavior. In some cases, death or coma can follow. Reye’s syndrome mostly affects children and teenagers, using aspirin during infection can increase this risk. VZV is closely related to the herpes simplex viruses (HSV), sharing much genome homology. The known envelope glycoproteins (gB, gC, gE, gH, gI, gK, gL) correspond with those in HSV; however, there is no equivalent of HSV gD. VZV also fails to produce the LAT (latency-associated transcripts) that play an important role in establishing HSV latency (herpes simplex virus). VZV virons are spherical and 180–200 nm in diameter. Their lipid envelope encloses the 100 nm nucleocapsid of 162 hexameric and pentameric capsomeres arranged in an icosahedral form. Its DNA is a single, linear, double-stranded molecule, 125,000 nt long. The capsid is surrounded by loosely associated proteins known collectively as the tegument; many of these proteins play critical roles in initiating the process of virus reproduction in the infected cell. The tegument is in turn covered by a lipid envelope studded with glycoproteins that are displayed on the exterior of the virion, each approximately 8 nm long. The genome was first sequenced in 1986. It is a linear duplex DNA molecule, a laboratory strain has 124,884 base pairs. The genome has 2 predominant isomers, depending on the orientation of the S segment, P (prototype) and IS (inverted S) which are present with equal frequency for a total frequency of 90–95%. The L segment can also be inverted resulting in a total of four linear isomers (IL and ILS). This is distinct from HSV's equiprobable distribution, and the discriminatory mechanism is not known. A small percentage of isolated molecules are circular genomes, about which little is known. (It is known that HSV circularizes on infection.) There are at least 70 open reading frames in the genome. There are at least five clades of this virus. Clades 1 and 3 include European/North American strains; clade 2 are Asian strains, especially from Japan; and clade 5 appears to be based in India. Clade 4 includes some strains from Europe but its geographic origins need further clarification.